Potpeschnigg observed a symmetrical gangrene of both hands in the case of a tNvo-year-old child three months after the onset of the scarlet fever. The condition began during the sixth week of the disease (Fig. 60).
Re/opse. —In order to diagnose a relapse, it is absolutely essential and necessary to establish the fact that there was a primary attack of scarlet fever. The diagnosis is justified only when it is certain that there was a characteristic eruption, and in the presence of other signs (angina, raspberry tongue), or when the scarlatinous nature of the disease is evidenced by tion, nephritis or the tion of other persons.
Caroline R., ten years old. Mild attack of scar let fever. Typical erup tion; pharynx red; rasp berry tongue; desquama tion.
Temperature normal after the fourth (lay.
On the eighteenth day, reddening of the left tonsil and left anterior fau cial pillar. On the former, a white spot the size of a lentil. Patient vomited four times in the course of the day; in the evening, pulse 140 (otherwise 90); angina. On the following morning typical eruption. Spot on tonsil increased in size; pharyngeal reddening more intense. Palpation tenderness of lymph-nodes at angle of jaw. Temperature, 3S.5° C. (101° F.) Eruption increased in intensity until fourth day; then receded rapidly. Second desquamation. Recovery.
Relapses have occurred from the eighteenth to the thirty-ninth day (Fig. 61).
The second attack may he much more severe than the first ; it may be accompanied by all the complications mentioned, and followed by a nephritis.
Aurelia Sch., eleven and a half years old. Cndoubted scarlet fever. Desquamation.
Typical searlatinal eruption on thirty-seventh day, with angina; joint pains. After convalescence, swelling of lymph-nodes, otitis and a severe hemorrhagic nephritis on sixtieth day after the onset of the first attack, and twenty-one days after the onset of the relapse.
During the third and fourth weeks of the disease one may observe angina without any eruption, simulating closely the angina of the pri mary attack. The accompanying temperature curve is also very similar to the original one. In two cases I observed redness and swelling of the pharynx synchronous with a nephritis; in one case angina was accom panied by a synovitis post-scarlatinosa.
A rather remarkable observation, one which may be made in all post-scarlatinal affections, is the occurrence of a symptomless interval between the primary symptoms of the disease and the appearance of the sequel ze.
Older theories as to the cause of the nephritis ascribe this as being due to chilling, irritation of the kidney by food, excessive strain of the kidney function owing to the damage done by the disease to the skin capillaries (mechanical theory of Bohn), and to the late excretion of toxins (Leichtenstern). Only the latter theory has met with favor, but it does not by any means account for the occurrence of the other sequela'. I have come to the conclusion that the real connection between the sequelte and the primary disease is about as follows: The exciting causes of the specific sequehe of scarlet fever (whether the cause of the disease itself or micro-organisms responsible for second ary infections) spread throughout the organism and finally their further development is checked. At the time that the sequelie make their ap pearance there is a diminished resistance of the body, or even a hyper sensitiveness, and the micro-organisms which have lodged in the various organs of the body are no longer inhibited in their growth. They resume their original activity, and such activity is manifested in part by toxic and again by infectious symptoms. Then, again, there is the possibility of a reinfection. It must be assumed, therefore, that at the end of the second week of the disease there exists a specific predisposition to post scarlatinal affections, which continues until about the seventh week. The greatest tendency to a lighting-up of these processes is seen during the third and fourth week, after which time such tendency diminishes perceptibly and rapidly.
Even this theory does not fully explain the genesis of the sequehe. The conception of a convalescence after scarlet fever must be based on something more than is usually done. The duration of the disease must 1w conceded to be for a longer time than is indicated by the usual clinical history of the disease. The predisposition to further manifestations, such as the occurrence of sequelre, must be considered as being a part of the original disease, and complete convalescence can not be said to have taken place until after this period of predisposition has been passed.